alcohol

Is it possible to have acute pancreatitis with normal serum lipase?

FA Manian MD, MPH, , , , , , Leave a comment

Yes! Although an elevated serum lipase has a negative predictive value of 94%-100% for acute pancreatitis (1), there are ample reports in the literature of patients with CT findings of pancreatitis in the presence of abdominal symptoms but with normal serum lipase and/or amylase (2,3).

A case series and review of literature of acute pancreatitis with normal lipase and amylase failed to reveal any specific risk factors for such observation (2). More specifically, the etiologies of acute pancreatitis in the reported cases have varied, including drug-induced, cholelithiasis, alcohol, hypertriglyceridemia, and postoperative causes.

But what accounts for this phenomenon? Many cases have been associated with the first bout of pancreatitis without evidence of pancreatic calcifications which makes the possibility of a “burned-out” pancreas without sufficient acinar cells to release lipase as a frequent cause unlikely. Other potential explanations for normal lipase in acute pancreatitis have included measurement of serum lipase at a very early phase of the disease before significant destruction of acinar cells has occurred (increases in 3-6 h, peaks at 24 h [4]) and more rapid renal clearance of serum lipase due to tubular dysfunction (2).

Of note, unlike amylase, lipase is totally reabsorbed by renal tubules under normal conditions (5). Thus, it’s conceivable that even a reversible tubular dysfunction may lead to increased clearance of serum lipase and potentially lower its levels.

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References
1. Ko K, Tello LC, Salt J. Acute pancreatitis with normal amylase and lipase. The Medicine Forum. 2011;11 Article 4. https://jdc.jefferson.edu/tmf/vol11/iss1/4/
2. Singh A, Shrestha M. Acute pancreatitis with normal amylase and lipase-an ED dilemma. Am J Emerg Med 2016;940.e5-940.e7. https://www.ncbi.nlm.nih.gov/pubmed/26521195
3. Limon O, Sahin E, Kantar FU, et al. A rare entity in ED: normal lipase level in acute pancreatitis. Turk J Emerg Med 2016;16:32-34. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4882216/
4. Shah AM, Eddi R, Kothari ST, et al. Acute pancreatitis with normal serum lipase: a case series. J Pancreas (Online) 2010 July 5;11:369-72. PDF
5. Lott JA, Lu CJ. Lipase isoforms and amylase isoenzymes: assays and application in the diagnosis of acute pancreatitis. Clin Chem 1991;37:361-68. https://www.ncbi.nlm.nih.gov/pubmed/1706232

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers, Mass General Hospital, Harvard Medical School or its affiliated institutions. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Is it possible to have acute pancreatitis with normal serum lipase?

My 35 year old patient with chronic alcoholism blames benign prostatic hypertrophy for his difficulty voiding. Could his bladder dysfunction be related to his alcoholism?

FA Manian MD, MPH, , , Leave a comment

Several case reports in the literature have stressed the association of bladder dysfunction (BD) with chronic alcohol abuse1,2.  Although some cases may be associated with concurrent thiamine deficiency (with its attendant neuropathy), other cases of BD do not appear to be. The mechanism of BD in this setting may be related to the toxic effect of alcohol on peripheral, autonomic and/or central nervous systems2,3.

Binge drinking may also be associated with urinary retention, with spontaneous atraumatic urinary bladder rupture having been reported on several occasions4. Lastly, alcohol withdrawal alone may precipitate urinary retention5.  

Unfortunately, many cases of abdominal pain due to urinary retention in the setting of alcohol abuse or withdrawal may be mistakenly attributed to ascites or other causes5.  High index of suspicion for BD is essential to minimize its complications.

In our patient, given the low prevalence of benign prostatic hypertrophy in men less than 40 years of age, urinary retention due to alcohol-related BD is more likely.

 

References

  1. Yuan R, Carcciolo VJ, Kulaga M. Chronic abdominal distension secondary to urinary retention in a patient with alcoholism. JAMA 2002;287;318-19.
  2. Sheremata WA, Sherwin I. Alcoholic myelopathy with spastic urinary bladder. Dis Nerv Syst 1972;33:136-139.
  3. Mellion M, Gilchrist JM, De La Monte S. Alcohol-related peripheral neuropathy: nutritional, toxic or both? Muscle Nerve 2011;43:309-16.
  4. Muneer M, Abdelrahman H, El-Menyar A, et al. Spontaneous atraumatic urinary bladder rupture secondary to alcohol intoxication: a case report and review of literature. Am J Case Rep 2015;16:778-81.
  5. Iga J-I, Taniguchi T, Ohmori T. Acute abdominal distension secondary to urinary retention in a patient after alcohol withdrawal. Alcohol Alcoholism 2005;40:86-87.
My 35 year old patient with chronic alcoholism blames benign prostatic hypertrophy for his difficulty voiding. Could his bladder dysfunction be related to his alcoholism?

My patient with chronic alcoholism is showing signs of alcohol withdrawal even though his blood alcohol level (BAL) is still elevated. Is this possible?

FA Manian MD, MPH, , , , , , Leave a comment

Absolutely! For patients with chronic alcohol dependence, any acute decline in their BAL may precipitate withdrawal (1).

For example, if a patient typically drinks enough alcohol on a daily basis to sustain a BAL of 350 mg/dl, any significant drop in BAL (e.g. down to 125 mg/dl) may be associated with early signs of withdrawal such as nervousness, tachycardia and elevated blood pressure.

Another scenario that could lead to withdrawal symptoms despite an elevated BAL involves patients who use both alcohol and benzodiazepines chronically. In such patients— because the 2 substances have cross-reactive effects on the brain— a significant reduction in the dose or frequency of benzodiazepines may also lead to withdrawal despite an elevated BAL.  Also remember that symptoms of benzodiazepine withdrawal may begin within 24 h or up to 2 weeks following its cessation (2).

Liked this post? Sign up under MENU and catch future pearls right into your inbox!

Reference

  1. Roffman JL, Stern TA.  Alcohol withdrawal in the setting of elevated blood alcohol levels. Prim Care Companion J Clin Psychiatry. 2006; 8(3):170-173 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1540391/
  2. Greenberg MI. Benzodiazepine withdrawal: potentially fatal, commonly missed, Emergency Medicine News 2001;23:18. https://journals.lww.com/em-news/pages/articleviewer.aspx?year=2001&issue=12000&article=00013&type=Fulltext

 

Contributed by Stephanie Meller, MD, Boston, MA

 

 

My patient with chronic alcoholism is showing signs of alcohol withdrawal even though his blood alcohol level (BAL) is still elevated. Is this possible?

Why is serum AST levels generally higher than ALT in alcohol-induced liver injury?

FA Manian MD, MPH, , Leave a comment

Alcohol is thought to cause injury to the mitochondria which contains AST but not ALT. In addition, in chronic alcoholics, pyridoxine (vitamin B6) deficiency may reduce the synthesis of ALT more than AST because the former is more B6-dependent (1).  

AST/ALT ratio >1 may be more common in advanced alcohol liver disease (e.g. cirrhosis) than in the setting of high alcohol consumption without severe liver disease (2). 

Also, remember that AST levels greater than 500 U/L and ALT levels greater than 300 U/L are uncommon in alcohol-related liver injury.  In this setting, other causes such as acetaminophen toxicity should be excluded (1).

References

1. Johnston DE. Special considerations in interpreting liver function tests. Am Fam Physician1999;59:2223-30.  https://www.ncbi.nlm.nih.gov/pubmed/10221307  

2. Nyblom H, Berggren U, Balldin J, et al. High AST/ALT ratio may indicate advanced alcoholic liver disease rather than heavy drinking. Alcohol &Alcoholism 2004;39:336-39. https://www.ncbi.nlm.nih.gov/pubmed/15208167

Why is serum AST levels generally higher than ALT in alcohol-induced liver injury?

Is there a connection between cirrhosis and elevated CK or rhabdomyolysis?

FA Manian MD, MPH, , , , , , , Leave a comment

Besides the usual causes of rhabdomyolysis such as trauma, drugs, alcohol, sepsis, etc…, cirrhotic patients may also have what some have called “hepatic myopathy”.  

One study involving 99 patients with cirrhosis and myopathy (all with elevated serum myoglobin) found “infections” as the most common cause (47%),  followed by “idiopathic” (27%) sources as well as ETOH, herbal medicine, and trauma-related causes (<10% each) (1).  Whether this is truly an entity  or just a non-causal association is unclear.

Another study reported that ~60% of rhabdomyolysis cases in cirrhosis had no apparent cause (2), with mortality among patient with cirrhosis and rhabdomyolysis significantly higher than that of controls without cirrhosis (27.5% vs 14.5%).

So perhaps we should lower our threshold for checking serum CK in our patients with cirrhosis and weakness.

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

Reference

1. Lee O-J, Yoon J-H, Lee E-J, et al. Acute myopathy associated with liver cirrhosis. World J Gastroenterol 2006;12:2254-2258.  https://www.ncbi.nlm.nih.gov/pubmed/16610032 .

2. Baek JE, Park DJ, Kim HJ, et al. The clinical characteristics of rhabdomyolysis in patients with liver cirrhosis. J Clin Gastroenterol 2007;41:317-21.

 

Is there a connection between cirrhosis and elevated CK or rhabdomyolysis?